Thermal Dehydrogenation Impact on Positive Bias Stability of Amorphous InSnZnO Thin-Film Transistors.

Recently, the growing demand for amorphous oxide semiconductor thin-film transistors (AOS TFTs) with high mobility and good stability to implement ultrahigh-resolution displays has made tracking the role of hydrogen in oxide semiconductor films increasingly important. Hydrogen is an essential element that contributes significantly to the field effect mobility and bias stability characteristics of AOS TFTs. However, because hydrogen is the lightest atom and has high reactivity to metal and oxide materials, elucidating its impact on AOS thin films has been challenging. Therefore, in this study, we propose controlling the hydrogen quantities in amorphous InSnZnO (a-ITZO) thin films through thermal dehydrogenation to precisely reveal the hydrogen influences on the electrical characteristics of a-ITZO TFTs. The as-deposited device containing 15.69 × 1015 atoms/cm2 of hydrogen exhibited a relatively low saturation mobility of 18.1 cm2/V·s and poor positive bias stress stability. However, depending on the extent of thermal dehydrogenation, not only did the hydrogen quantity and interface defect density (DIT) decrease but also the conductivity and surface energy increased due to the rise in oxygen vacancies and hydroxyl groups in a-ITZO thin films. As a result, the a-ITZO TFT with a hydrogen amount of 4.828 × 1015 atoms/cm2 showed that the saturation mobility improved up to 36.8 cm2/V·s, and positive bias stress stability was remarkably enhanced. Hence, we report the ability to manage the hydrogen quantity with thermal dehydrogenation and demonstrate that high-performance a-ITZO TFTs can be realized when an appropriate hydrogen concentration is achieved.

APOE3-R136S mutation confers resilience against tau pathology via cGAS-STING-IFN inhibition.

The Christchurch mutation (R136S) on the APOE3 (E3S/S) gene is associated with low tau pathology and slowdown of cognitive decline despite the causal PSEN1 mutation and high levels of amyloid beta pathology in the carrier1. However, the molecular effects enabling E3S/S mutation to confer protection remain unclear. Here, we replaced mouse Apoe with wild-type human E3 or E3S/S on a tauopathy background. The R136S mutation markedly mitigated tau load and protected against tau-induced synaptic loss, myelin loss, and spatial learning. Additionally, the R136S mutation reduced microglial interferon response to tau pathology both in vivo and in vitro, suppressing cGAS-STING activation. Treating tauopathy mice carrying wild-type E3 with cGAS inhibitor protected against tau-induced synaptic loss and induced similar transcriptomic alterations to those induced by the R136S mutation across brain cell types. Thus, cGAS-STING-IFN inhibition recapitulates the protective effects of R136S against tauopathy.